The objective of the research is to investigate those factors which regulate the reversible inactivation and reactivation of kidney sodium-potassium adenosine triphosphatase (ATPase). The data supports the hypothesis that renal ATPase is in part regulated by cyclic AMP dependent protein kinase. The current effort is to characterize the factor in the 100,000 xg cell cytosol which mediates the reacivation of ATPase inhibited by protein kinase. Recent evidence by various investigators has indicated that some commercial preparations of ATP are contaminated with vanadium. Vanadium is a potent inhibitor of ATPase. Work is in progress demonstrating that inhibition of ATPase by vanadium is a mechanism separate from the inhibition by protein kinase. The final objective of the research effort is to reconstitute the individually isolated inactivating and reactivating components of ATPase into an in vitro system with ATPase.